1. Articles in category: Drug Resistance

    1-18 of 18
    1. Palmitic acid stimulates energy metabolism and inhibits insulin/PI3K/AKT signaling in differentiated human neuroblastoma cells: The role of mTOR activation and mitochondrial ROS production.

      Palmitic acid stimulates energy metabolism and inhibits insulin/PI3K/AKT signaling in differentiated human neuroblastoma cells: The role of mTOR activation and mitochondrial ROS production.

      Neurochem Int. 2017 Sep 15;:

      Authors: Calvo-Ochoa E, Sánchez-Alegría K, Gómez-Inclán C, Ferrera P, Arias C

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    2. Annexin A2 could enhance multidrug resistance by regulating NF-κB signaling pathway in pediatric neuroblastoma.

      Annexin A2 could enhance multidrug resistance by regulating NF-κB signaling pathway in pediatric neuroblastoma.

      J Exp Clin Cancer Res. 2017 Aug 16;36(1):111

      Authors: Wang Y, Chen K, Cai Y, Cai Y, Yuan X, Wang L, Wu Z, Wu Y

      Abstract BACKGROUND: Chemotherapy is one of major therapeutic regimens for neuroblastoma (NB) in children. However, recurrence and metastasis associated with poor prognosis caused by acquired multidrug resistance remains a challenge.

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    3. Anti-cancer effect of oncolytic adenovirus-armed shRNA targeting MYCN gene on doxorubicin-resistant neuroblastoma cells.

      Anti-cancer effect of oncolytic adenovirus-armed shRNA targeting MYCN gene on doxorubicin-resistant neuroblastoma cells.

      Biochem Biophys Res Commun. 2017 Jul 12;:

      Authors: Li Y, Zhuo B, Yin Y, Han T, Li S, Li Z, Wang J

      Abstract Chemotherapy is one of the few effective choices for patients with neuroblastoma. However, the development of muti-drug resistance (MDR) to chemotherapy is a major obstacle to the effective treatment of advanced or recurrent neuroblastoma.

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    4. Oral Metronomic Topotecan Sensitizes Crizotinib Antitumor Activity in ALK(F1174L) Drug-Resistant Neuroblastoma Preclinical Models.

      Oral Metronomic Topotecan Sensitizes Crizotinib Antitumor Activity in ALK(F1174L) Drug-Resistant Neuroblastoma Preclinical Models.

      Transl Oncol. 2017 Jun 27;10(4):604-611

      Authors: Zhang L, Wu B, Baruchel S

      Abstract BACKGROUND: Anaplastic lymphoma kinase (ALK) inhibitor crizotinib has proven to be effective in the treatment of ALK-mutated neuroblastoma, but crizotinib resistance was commonly observed in patients.

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      Mentions: Treatment ALK
    5. SAHA sensitizes neuroblastoma to paclitaxel by inhibiting TRP14-mediated autophagy.

      SAHA sensitizes neuroblastoma to paclitaxel by inhibiting TRP14-mediated autophagy.

      Cancer Sci. 2017 May 12;:

      Authors: Zhen Z, Yang K, Ye L, You Z, Chen R, Liu Y, He Y

      Abstract Paclitaxel is not as effective for neuroblastoma as most of the front-line chemotherapeutics due to drug resistance. This study explored the regulatory mechanism of paclitaxel-associated autophagy and potential solutions to paclitaxel resistance in neuroblastoma.

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    6. Combined ALK and MDM2 inhibition increases antitumor activity and overcomes resistance in human ALK mutant neuroblastoma cell lines and xenograft models.

      Combined ALK and MDM2 inhibition increases antitumor activity and overcomes resistance in human ALK mutant neuroblastoma cell lines and xenograft models.

      Elife. 2017 Apr 20;6:

      Authors: Wang HQ, Halilovic E, Li X, Liang J, Cao Y, Rakiec DP, Ruddy DA, Jeay S, Wuerthner JU, Timple N, Kasibhatla S, Li N, Williams JA, Sellers WR, Huang A, Li F

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      Mentions: ALK MYCN
    7. YAP promotes tumorigenesis and cisplatin resistance in neuroblastoma.

      YAP promotes tumorigenesis and cisplatin resistance in neuroblastoma.

      Oncotarget. 2017 Mar 15;:

      Authors: Yang C, Tan J, Zhu J, Wang S, Wei G

      Abstract The transcriptional co-activator Yes-associated protein (YAP) is essential for Hippo pathway-driven tumorigenesis in various cancers. However, the expression and function of YAP in neuroblastoma remains elusive. Here, we show that YAP was highly expressed in Neuroblastoma (NB) and expression levels correlated with advanced tumor staging.

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    8. Overcoming drug resistance by cell-penetrating peptide-mediated delivery of a doxorubicin dimer with high DNA-binding affinity.

      Overcoming drug resistance by cell-penetrating peptide-mediated delivery of a doxorubicin dimer with high DNA-binding affinity.

      Eur J Med Chem. 2017 Feb 27;130:336-345

      Authors: Lelle M, Freidel C, Kaloyanova S, Tabujew I, Schramm A, Musheev M, Niehrs C, Müllen K, Peneva K

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    9. NDRG1 promotes the multidrug resistance of neuroblastoma cells with upregulated expression of drug resistant proteins.

      NDRG1 promotes the multidrug resistance of neuroblastoma cells with upregulated expression of drug resistant proteins.

      Biomed Pharmacother. 2015 Dec;76:46-51

      Authors: Zhang D, Jia J, Zhao G, Yue M, Yang H, Wang J

      Abstract BACKGROUND: Resistance to chemotherapeutic drugs and recurrence are two major causes of poor prognosis in many tumors including neuroblastoma.

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    10. PDK1-mTOR signaling pathway inhibitors reduce cell proliferation in MK2206 resistant neuroblastoma cells.

      PDK1-mTOR signaling pathway inhibitors reduce cell proliferation in MK2206 resistant neuroblastoma cells.

      Cancer Cell Int. 2015;15:91

      Authors: Qi L, Toyoda H, Xu DQ, Zhou Y, Sakurai N, Amano K, Kihira K, Hori H, Azuma E, Komada Y

      Abstract PURPOSE: AKT plays a pivotal role in the signal transduction of cancer cells. MK2206, an AKT inhibitor, has been shown to be an effective anti-cancer drug to a variety of cancer cell lines.

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    11. High mobility group box 1-mediated autophagy promotes neuroblastoma cell chemoresistance.

      High mobility group box 1-mediated autophagy promotes neuroblastoma cell chemoresistance.

      Oncol Rep. 2015 Sep 16;

      Authors: Wang L, Zhang H, Sun M, Yin Z, Qian J

      Abstract Neuroblastoma (NB) is one of the most common tumors in childhood. Unfortunately, the survival outcomes remain unsatisfactory since NB commonly develops multidrug resistance.

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    12. Vacuolar-ATPase-mediated intracellular sequestration of ellipticine contributes to drug resistance in neuroblastoma cells.

      Neuroblastoma is the most common cancer in infants and the fourth most common cancer in children. Aggressive cell growth and chemoresistance are notorious obstacles in neuroblastoma therapy. Exposure to the anticancer drug ellipticine inhibits efficiently growth of neuroblastoma cells and induces apoptosis in these cells. However, ellipticine induced resistance in these cells.

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    13. CD114 Expression Mediates Melanoma Tumor Cell Growth and Treatment Resistance.

      1Department of Pediatrics, Section of Hematology-Oncology, Texas Children's Cancer and Hematology Centers, Baylor College of Medicine, Houston, TX, U.S.A. 2Department of Pediatrics, Section of Hematology-Oncology, Texas Children's Cancer and Hematology Centers, Baylor College of Medicine, Houston, TX, U.S.A. zage@bcm.edu. Melanoma tumor cell sub-populations expressing a variety of specific molecular markers have been identified.

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      Mentions: Chemotherapy G-CSF
    14. Tackling Crizotinib Resistance: The Pathway from Drug Discovery to the Pediatric Clinic.

      1Paediatric Solid Tumour Biology and Therapeutics Team, Division of Cancer Therapeutics, The Institute of Cancer Research, London, United Kingdom. 2Cancer Research UK Cancer Therapeutics Unit, Division of Cancer Therapeutics, The Institute of Cancer Research, London, United Kingdom. 3Paediatric Solid Tumour Biology and Therapeutics Team, Division of Cancer Therapeutics, The Institute of Cancer Research, London, United Kingdom. Louis.Chesler@icr.ac.uk.

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      Mentions: ALK
    15. Resistance to the atypical retinoid ST1926 in SK-N-AS cells selected the subline rAS-ST with enhanced sensitivity to ATRA mediated by not conventional mechanisms: DNA damage, G2 accumulation and late telomerase inhibition.

      1Division of Paediatric Oncology, Catholic University of Rome, Rome, Italy. Electronic address: angeladifrancesco@tin.it. 2Division of Paediatric Oncology, Catholic University of Rome, Rome, Italy. 3Department of Systems Medicine, Section of Pharmacology, University of Rome "Tor Vergata", Italy. 4Department of Pharmacy and Biotechnology, University of Bologna, Bologna;Italy. 5Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.

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    1-18 of 18
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